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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...

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Related Experiment Video

Updated: May 19, 2026

Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism
11:04

Quantification of Global Diastolic Function by Kinematic Modeling-based Analysis of Transmitral Flow via the Parametrized Diastolic Filling Formalism

Published on: September 1, 2014

Molecular and cellular basis for diastolic dysfunction.

Loek van Heerebeek1, Constantijn P M Franssen, Nazha Hamdani

  • 1Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.

Current Heart Failure Reports
|August 29, 2012
PubMed
Summary
This summary is machine-generated.

Heart failure with preserved ejection fraction (HFpEF) involves stiffening of heart muscle cells, driven by changes in the titin protein. This stiffness contributes to diastolic dysfunction, impacting heart function in this common condition.

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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
09:20

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction

Published on: February 13, 2021

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is a prevalent condition often linked to metabolic risk factors.
  • HFpEF shares similar mortality rates with heart failure with reduced ejection fraction (HFrEF), highlighting its clinical significance.
  • The underlying pathophysiology of HFpEF remains incompletely understood, hindering the development of targeted therapies.

Purpose of the Study:

  • To elucidate the molecular mechanisms contributing to diastolic dysfunction in HFpEF.
  • To investigate the role of titin posttranslational modifications in cardiomyocyte stiffness within HFpEF.

Main Methods:

  • Analysis of cardiac remodeling at macroscopic, microscopic, and ultrastructural levels in HFpEF.
  • Assessment of cardiomyocyte and extracellular matrix contributions to diastolic stiffness.
  • Investigation of posttranslational modifications of titin, including isoform expression and phosphorylation.

Main Results:

  • Elevated intrinsic cardiomyocyte stiffness is a key factor in the increased diastolic left-ventricular (LV) stiffness observed in HFpEF.
  • Posttranslational changes in titin, specifically altered expression and phosphorylation, contribute significantly to cardiomyocyte stiffness.
  • Increased nitrosative/oxidative stress and impaired nitric oxide signaling pathways are implicated in triggering titin modifications.

Conclusions:

  • Posttranslational modifications of titin, influenced by oxidative stress and altered signaling, augment cardiomyocyte and LV diastolic stiffness in HFpEF.
  • Understanding these molecular changes in titin offers potential therapeutic targets for HFpEF.
  • Distinct cardiac remodeling processes in HFpEF contribute to diastolic dysfunction and impaired cardiac relaxation.